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. Author manuscript; available in PMC: 2014 Jul 23.
Published in final edited form as: Circulation. 2013 Jun 19;128(4):10.1161/CIRCULATIONAHA.113.003183. doi: 10.1161/CIRCULATIONAHA.113.003183

Figure 1.

Figure 1

Cardiac dysfunction in Myo-Tg mice is associated with βAR desensitization and is independent of sympathetic overdrive. (A) In vitro isoproterenol (I) (closed bars) stimulated cardiac adenylyl cyclase activity compared to vehicle (V) (open bars) in the Wt and Myo-Tg mice of 4, 8, 12, 16 and 36 weeks of age (n=6–8), *p< 0.001 versus respective I Wt, #p<0.01 versus I Wt (all ages) & I Myo (4 & 8 weeks). (B) A plot of correlation between adenylyl cyclase activity and % fractional shortening (% FS) in Wt and Myo-Tg mice. *p< 0.01 versus Wt, #p<0.05 versus Myo 4 & 8 weeks. (C) Plasma epinephrine levels of Wt and Myo-Tg mice at 8 and 12 weeks (n=5–7). (D) Plasma norepinephrine levels of Wt and Myo-Tg mice at 8 and 12 weeks (n=5–7). (E) Immunoblotting for GRK 2, 3, 5, 6 and β-actin from cardiac lysates of Wt and Myo-Tg mice at 4, 12, 16, and 36 weeks of age. (F) Summary data of densitometric analysis of GRK2 (n=6–8), *p< 0.001 versus Myo-Tg at 4 weeks.